Operant control of epileptic neurons in chronic foci of monkeys

(1) Six Macaca mulatta monkeys were rendered chronically epileptic by subpial alumina injection in left precentral cortex. The monkeys were then trained to operantly control the firing patterns of single units from the epileptic focus and contralateral homotopic cortex using a standardized paradigm. In 30 experiments, units were recorded simultaneously from both hemispheres. (2) For epileptic and normal neurons, there are no consistent relationships between cortical EEG spikes and unit firing. (3) Previous parameters for quantifying single unit epileptogenicity are not adequate for defining the complex spectrum and relative degree of unit abnormalities within the chronic focus. A primary difference between normal and epileptic neurons is that monkeys can modify the firing pattern and rate of the former but can modify, only slightly, the integrated firing rate of the latter. (4) A previously described 'non-burst' epileptiform firing pattern consisting of 8--18 msec doublets is investigated in further detail. This pattern may represent units along a continuum between normalcy and long-first-interval burst firing. (5) The majority of epileptic units' firing patterns become more normal when the monkey is reinforced to control the firing pattern of a contralateral unit. Then, if the monkey is reinforced to control the epileptic unit, subtle abnormal firing patterns become more apparent. Therefore, the firing patterns of epileptic units are effected in two ways: the non-specific effect of alerting to the operant task, and the more specific effect that accompanies the monkey's attempts to attain reinforcement when it is contingent on the behavior of the specific neuron. (6) Although epileptiform EEG spikes are projected to homotopic contralateral precentral cortex, there is no evidence to suggest that single units within such cortex fire in patterns correlative with intrinsic epileptogenic burst generating properties. Therefore, if the 'mirror focus' is defined as cortex which has become autonomously epileptogenic secondary to persistent transsynaptic activity from a primary focus, these data do not support the concept that mirror foci develop in primate precentral cortex.